Reward-related memory and interindividual variability in structural and functional brain networks

On any given day we only remember a fraction of what we experience. An event’s salience will influence the probability of remembering. Extrinsic reward has been shown to introduce salience and facilitate memory. Yet, memory modulation through reward varies between individuals. This thesis aims to investigate: the brain networks associated with variability in reward-modulated memory; how reward influences hippocampus-dependent memory such as recollection, temporal order, and associative memory; how reward influences consolidation of intentionally memorised information; and how variability within brain networks associated with rewarded memory formation relates to variability in the influence of reward on different types of memory. Chapter 2 examined the effect of reward on temporal order memory and whether this effect was dependent on the type of post-encoding period. Comparing a distractor and a wakeful rest, temporal order memory was better for high than low reward items only when a distractor task filled the post-encoding period. Chapters 3 and 4 investigated the structural and functional connections underlying variability in reward-modulated temporal order memory. In Chapter 3, variability in the reward-related enhancement of temporal order memory was found to be associated with variability in the microstructure of the right inferior longitudinal fasciculus. Chapter 4 indicated a relationship between resting-state functional connectivity within a right hemispheric semantic network and variability in the reward-related temporal order memory benefit. Chapters 5 and 6 investigated the structural and functional connections underlying variability in immediate versus 24-hour delayed intentional memory. In Chapter 5, variability in delayed memory was related to variability in fornix microstructure. Chapter 6 indicated a relationship between variability in reward-related memory enhancement at delayed memory test and variability in resting-state functional connectivity between nucleus accumbens and hippocampus. Together, these findings contribute to a better understanding of how individual variability in structural and functional connections relate to reward-modulated memory enhancements

Curiosity and mesolimbic functional connectivity drive information seeking in real life

Curiosity reflects an individual’s intrinsic motivation to seek information in order to close information gaps. In laboratory-based experiments, both curiosity and information seeking have been associated with enhanced neural dynamics in the mesolimbic dopaminergic circuit. However, it is unclear whether curiosity and dopaminergic dynamics drive information seeking in real life. We investigated (i) whether curiosity predicts different characteristics of real-life information seeking and (ii) whether functional connectivity within the mesolimbic dopaminergic circuit is associated with information seeking outside the laboratory. Up to 15 months before the COVID-19 pandemic, curiosity and anxiety questionnaires and a 10-minute resting-state functional magnetic resonance imaging session were conducted. In a follow-up survey early during the COVID-19 pandemic, participants repeated the questionnaires and completed an additional questionnaire about their COVID-19-related information seeking. Individual differences in curiosity but not anxiety were positively associated with the frequency of information-seeking behaviour. Additionally, the frequency of information seeking was predicted by individual differences in resting-state functional connectivity between the ventral tegmental area and the nucleus accumbens. The present translational study paves the way for future studies on the role of curiosity in real-life information seeking by showing that both curiosity and the mesolimbic dopaminergic functional network support real-life information-seeking behaviour

Brief learning induces a memory bias for arousing-negative words: an fMRI study in high and low trait anxious persons

Eden AS, Dehmelt V, Bischoff M, et al. Brief learning induces a memory bias for arousing-negative words: an fMRI study in high and low trait anxious persons. Frontiers in Psychology. 2015;6: 1226.Persons suffering from anxiety disorders display facilitated processing of arousing and negative stimuli, such as negative words. This memory bias is reflected in better recall and increased amygdala activity in response to such stimuli. However, individual learning histories were not considered in most studies, a concern that we meet here. Thirty-four female persons (half with high-, half with low trait anxiety) participated in a criterion-based associative word-learning paradigm, in which neutral pseudowords were paired with aversive or neutral pictures, which should lead to a valence change for the negatively paired pseudowords. After learning, pseudowords were tested with fMRI to investigate differential brain activation of the amygdala evoked by the newly acquired valence. Explicit and implicit memory was assessed directly after training and in three follow-ups at 4-day intervals. The behavioral results demonstrate that associative word-learning leads to an explicit (but no implicit) memory bias for negatively linked pseudowords, relative to neutral ones, which confirms earlier studies. Bilateral amygdala activation underlines the behavioral effect: Higher trait anxiety is correlated with stronger amygdala activation for negatively linked pseudowords than for neutrally linked ones. Most interestingly, this effect is also present for negatively paired pseudowords that participants could not remember well. Moreover, neutrally paired pseudowords evoked higher amygdala reactivity than completely novel ones in highly anxious persons, which can be taken as evidence for generalization. These findings demonstrate that few word-learning trials generate a memory bias for emotional stimuli, indexed both behaviorally and neurophysiologically. Importantly, the typical memory bias for emotional stimuli and the generalization to neutral ones is larger in high anxious persons

Association of retinal vessel pathology and brain atrophy in relapsing-remitting multiple sclerosis

BackgroundOptical coherence tomography angiography (OCTA) allows non-invasive assessment of retinal vessel structures. Thinning and loss of retinal vessels is evident in eyes of patients with multiple sclerosis (MS) and might be associated with a proinflammatory disease phenotype and worse prognosis. We investigated whether changes of the retinal vasculature are linked to brain atrophy and disability in MS.Material and methodsThis study includes one longitudinal observational cohort (n=79) of patients with relapsing-remitting MS. Patients underwent annual assessment of the expanded disability status scale (EDSS), timed 25-foot walk, symbol digit modalities test (SDMT), retinal optical coherence tomography (OCT), OCTA, and brain MRI during a follow-up duration of at least 20 months. We investigated intra-individual associations between changes in the retinal architecture, vasculature, brain atrophy and disability. Eyes with a history of optic neuritis (ON) were excluded.ResultsWe included 79 patients with a median disease duration of 12 (interquartile range 2 - 49) months and a median EDSS of 1.0 (0 - 2.0). Longitudinal retinal axonal and ganglion cell loss were linked to grey matter atrophy, cortical atrophy, and volume loss of the putamen. We observed an association between vessel loss of the superficial vascular complex (SVC) and both grey and white matter atrophy. Both observations were independent of retinal ganglion cell loss. Moreover, patients with worsening of the EDSS and SDMT revealed a pronounced longitudinal rarefication of the SVC and the deep vascular complex.DiscussionON-independent narrowing of the retinal vasculature might be linked to brain atrophy and disability in MS. Our findings suggest that retinal OCTA might be a new tool for monitoring neurodegeneration during MS

Inclusive V0V^0 Production Cross Sections from 920 GeV Fixed Target Proton-Nucleus Collisions

Inclusive differential cross sections $d\sigma_{pA}/dx_F$ and $d\sigma_{pA}/dp_t^2$ for the production of \kzeros, \lambdazero, and \antilambda particles are measured at HERA in proton-induced reactions on C, Al, Ti, and W targets. The incident beam energy is 920 GeV, corresponding to $\sqrt {s} = 41.6$ GeV in the proton-nucleon system. The ratios of differential cross sections \rklpa and \rllpa are measured to be $6.2\pm 0.5$ and $0.66\pm 0.07$, respectively, for \xf $\approx-0.06$. No significant dependence upon the target material is observed. Within errors, the slopes of the transverse momentum distributions $d\sigma_{pA}/dp_t^2$ also show no significant dependence upon the target material. The dependence of the extrapolated total cross sections $\sigma_{pA}$ on the atomic mass $A$ of the target material is discussed, and the deduced cross sections per nucleon $\sigma_{pN}$ are compared with results obtained at other energies.Comment: 17 pages, 7 figures, 5 table

The QCD transition temperature: results with physical masses in the continuum limit II.

We extend our previous study [Phys. Lett. B643 (2006) 46] of the cross-over temperatures (T_c) of QCD. We improve our zero temperature analysis by using physical quark masses and finer lattices. In addition to the kaon decay constant used for scale setting we determine four quantities (masses of the \Omega baryon, K^*(892) and \phi(1020) mesons and the pion decay constant) which are found to agree with experiment. This implies that --independently of which of these quantities is used to set the overall scale-- the same results are obtained within a few percent. At finite temperature we use finer lattices down to a <= 0.1 fm (N_t=12 and N_t=16 at one point). Our new results confirm completely our previous findings. We compare the results with those of the 'hotQCD' collaboration.Comment: 19 pages, 8 figures, 3 table

Temporal proximity to the elicitation of curiosity is key for enhancing memory for incidental information

Curiosity states benefit memory for curiosity target information, but also incidental information presented during curiosity states. Curiosity-related activity in dopaminergic regions and the hippocampus predicts such curiosity-enhanced memory for incidental information. However, it is not known whether incidental curiosity-enhanced memory depends on when incidental information during curiosity states is encountered. Here, participants incidentally encoded unrelated face images at different time points while they anticipated answers to trivia questions. Across two experiments, we found memory enhancements for unrelated faces presented during high- compared to low-curiosity states, but only when a face was presented shortly after a trivia question. This incidental curiosity-enhanced memory was independent of the type of encoding judgement and was evident both after a short (Experiment 1) and a 24-hour delay (Experiment 2). The findings suggest that processes associated with the elicitation of curiosity - but not processes preceding the satisfaction of curiosity - enhance memory for incidental information

Temporal proximity to the elicitation of curiosity is key for enhancing memory for incidental information

Curiosity states benefit memory for target information, but also incidental information presented during curiosity states. However, it is not known whether incidental curiosity-enhanced memory depends on when incidental information during curiosity states is encountered. Here, participants incidentally encoded unrelated face images at different time points while they anticipated answers to trivia questions. Across two experiments, we found memory enhancements for unrelated faces presented during high-curiosity compared with low-curiosity states, but only when presented shortly after a trivia question. This suggests processes associated with the elicitation of curiosity—but not sustained anticipation or the satisfaction of curiosity—enhance memory for incidental information

A novel mouse model with impaired dynein/dynactin function develops amyotrophic lateral sclerosis (ALS)-like features in motor neurons and improves lifespan in SOD1-ALS mice

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative condition characterized by progressive motor neuron degeneration and muscle paralysis. Genetic evidence from man and mouse has indicated that mutations in the dynein/dynactin motor complex are correlated with motor neuron degeneration. In this study, we have generated transgenic mice with neuron-specific expression of Bicaudal D2 N-terminus (BICD2-N) to chronically impair dynein/dynactin function. Motor neurons expressing BICD2-N showed accumulation of dynein and dynactin in the cell body, Golgi fragmentation and several signs of impaired retrograde trafficking: the appearance of giant neurofilament swellings in the proximal axon, reduced retrograde labelling by tracer injected in the muscle and delayed expression of the injury transcription factor ATF3 after axon transection. Despite these abnormalities, BICD2-N mice did not develop signs of motor neuron degeneration and motor abnormalities. Interestingly, the BICD2-N transgene increased lifespan in 'low copy' SOD1-G93A ALS transgenic mice. Our findings indicate that impaired dynein/dynactin function can explain several pathological features observed in ALS patients, but may be beneficial in some forms of ALS